This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.

Many systemic diseases can develop oral manifestations that may include gingival enlargement, some that are related to conditions and others that are related to disease:

- Conditioned enlargement

- pregnancy

- puberty

- vitamin C deficiency

- nonspecific, such as a pyogenic granuloma

- Systemic disease causing enlargement

- leukemia

- granulolomatous diseases, such as granulomatosis with polyangiitis, sarcoidosis, or orofacial granulomatosis.

- neoplasm

- benign neoplasms, such as fibromas, papillomas and giant cell granulomas

- malignant neoplasms, such as a carcinoma or malignant melanoma

- false gingival enlargements, such as when there is an underlying bony or dental tissue lesion

This condition occurs in association with denture wearing, and so those affected tend to be middle aged or older adults. 66-75% are estimated to occur in women. Epulis fissuratum is the third most common reactive lesion that occurs in the mouth, after peripheral giant cell granuloma and pyogenic granuloma.

If the causative factor persists, tissue will become more fibrous over time.

Drug-related gingival hyperplasia is a cutaneous condition characterized by enlargement of the gums noted during the first year of drug treatment. There are three drug classes that are associated with this condition namely, anticonvulsants (such as phenyotoin and phenobartibal), calcium channel blocker (such as amlopidine, nifedipine and verapamil) and ciclosporin, an immunosuppressant Although the mechanism of drug related gingival hyperplasia is not well understood, some risk factors for the condition include the duration of drug use and poor oral hygiene. In most cases, alternative drugs are given, in order to avoid this side effect.

Also termed a "pregnancy tumor" or "granuloma gravidarum", this lesion is identical to a pyogenic granuloma in all respects apart from the fact that it occurs exclusively in pregnant females. There is usually pregnancy gingivitis also. Pregnancy epulis commonly occurs during the third trimester of pregnancy.

This is a fibrous hyperplasia of excess connective tissue folds that takes place in reaction to chronic trauma from an ill fitting denture. It usually occurs in the mandibular labial sulcus. Sometimes the term "epulis" is used synonymously with epulis fissuratum, but this is technically incorrect as several other lesions could be described as epulides.

Hyperplasia may be due to any number of causes, including increased demand (for example, proliferation of basal layer of epidermis to compensate skin loss), chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere. Hyperplasia may be harmless and occur on a particular tissue. An example of a normal hyperplastic response would be the growth and multiplication of milk-secreting glandular cells in the breast as a response to pregnancy, thus preparing for future breast feeding.

Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells. By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and steroid use and is simply an increase in the size of the cells. With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue. Weight training with or without anabolic steroid use enables these new cells to mature in size and strength. It is theorized that hyperplasia may also be induced through specific power output training for athletic performance, thus increasing the number of muscle fibers instead of increasing the size of a single fiber.

Treatment usually involves surgical removal of the lesion down to the bone. If there are any adjacent teeth, they are cleaned thoroughly to remove any possible source of irritation. Recurrence is around 16%.

Some of the more commonly known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:

- Benign prostatic hyperplasia, also known as prostate enlargement.

- Cushing's disease – Physiopathology of hyperplasia of adrenal cortex due to increased circulating level of ACTH (adrenocorticotropic hormone).

- Congenital adrenal hyperplasia – Inherited disorder of gland (adrenal).

- Endometrial hyperplasia – Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma. The development of endometrial adenocarcinoma from endometrial hyperplasia is a typical example of how the effects of pathologic hyperplasia can lead to neoplasia, and females who exhibit hyperplasia of the endometrium are indeed more likely to develop cancer of these cells.

- Hemihyperplasia when only half (or one side) of the body is affected, sometimes generating limbs of different lengths.

- Hyperplasia of the breast – "Hyperplastic" lesions of the breast include "usual ductal hyperplasia", a focal expansion of the number of cells in a terminal breast duct, and "atypical ductal hyperplasia", in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer.

- Intimal hyperplasia – The thickening of the tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy. Intimal hyperplasia is the universal response of a vessel to injury and is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.

- Focal epithelial hyperplasia (also known as Heck's disease) – This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck's disease has not been known to cause cancer.

- Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.

- Compensatory liver hyperplasia – The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, i.e., hyperplasia. This is what makes living-donor liver transplants possible.

There are many possible causes of gingival bleeding. The main cause of gingival bleeding is the formation and accumulation of plaque at the gum line due to improper brushing and flossing of teeth. The hardened form of plaque is calculus. An advanced form of gingivitis as a result of formation of plaque is periodontitis. Other causes that can exacerbate gingival bleeding include:

- placement of new dentures

- tooth or gum infection

- diabetes mellitus

- idiopathic thrombocytopenic purpura

- leukemia

- malnutrition

- use of aspirin and anticoagulants(blood thinners) such as warfarin and heparin

- hormonal imbalances during puberty and pregnancy

- iron overload

Other less common causes are:

- vitamin C deficiency (scurvy) and vitamin K deficiency

- dengue fever

Some researchers suggest that HGF is transmitted as a Mendelian trait since both autosomal dominant and autosomal recessive transmission has been reported since the early 1970s. (SOURCE 1) In more recent scientific literature, there is evidence in which pedigree analyses confirm autosomal dominant, autosomal recessive or even as X-linked inherited cases of the HGF trait.

In 2002, researchers described the SOS1 gene and proved for the first time that a single-nucleotide–insertion mutation of the SOS1 gene on codon 1083 is the preliminary cause of HGF1 in humans. (Source 1) Later on in 2010, there was a case study done on a 16-year-old male with severe gingival overgrowth, almost covering all teeth. Researchers approached this issue with periodontics - a partial gingivectomy and flap surgery. This case study concluded that surgery followed by regular follow-ups is a good way to treat HGF despite the fact that the risks of re-occurrence of the condition remain high.

Even more recently, a study was done in 2013 on a family that showed history of autosomal recessive inheritance of HGF. The study did not dismiss the return of HGF after treatment but did claim that general surgical intervention after scaling and root planning of teeth supplemented with good oral hygiene is good enough to prevent the re-occurrence of HGF. This case study also acknowledged how HGF can be part of a multi-system syndrome associated with disorders such as Zimmermann Laband syndrome (ear, nose, bone, and nail defects with hepatosplenomegaly), Rutherford syndrome (microphthalmia, mental retardation, athetosis, and hypopigmentation), Murray-Puretic Drescher syndrome and Ramon syndrome.

The following can occur if left untreated:

- Too much gingiva exposure

- Oral morbidity

- Chronic infection of areas between the gums and teeth, or at the gum line

- various degrees of Periodontitis - most likely due to the inability and difficulty of keeping the gingival margin and surrounding tissue clean due to the overgrowth

- Improper tooth eruption and/or complete prevention of tooth eruption as a result of too much gingiva exposure

- Systemic every-day troubles including functional and aesthetic problems of the mouth

- Malocclusion

Salivary gland hyperplasia is hyperplasia of the terminal duct of salivary glands.

There are two types:

- Acinar adenomatoid hyperplasia

- Ductal adenomatoid hyperplasia

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Peripheral ossifying fibroma “a gingival nodule which is composed of a cellular fibroblastic connective tissue stroma which is associated with the formation of randomly dispersed foci of mineralised products, which consists of bone, cementum-like tissue, or a dystrophic calcification. The lesion is considered part of an ossifying fibroma, but that is usually considered to be a gnathic tumor. Because of its overwhelming incidence on the gingiva, the condition is associated with two other diseases, though not because they occur together. Instead, the three are associated with each other because they appear frequently on gingiva: pyogenic granuloma and peripheral giant cell granuloma. Some researchers believe peripheral ossifying fibromas to be related to pyogenic fibromas and, in some instances, are the result of a pyogenic granuloma which has undergone fibrosis and calcification.

The term "peripheral ossifying fibroma" has been criticized as this lesion is not related to the ossifying fibroma of bone and is not a fibroma. This term is used in America, however in Britain, this lesion would be termed a fibrous epulis containing bone.

Risk factors associated with gingivitis include the following:

- age

- osteoporosis

- low dental care utilization (fear, financial stresses, etc.)

- poor oral hygiene

- overly aggressive oral hygiene such as brushing with stiff bristles

- mouth-breathing during sleep

- medications that dry the mouth

- cigarette smoking

- genetic factors

- pre-existing conditions

The peripheral odontogenic fibroma is an uncommon gingival mass. It affects people across a large age range. It can be confused with the peripheral ossifying fibroma. In contrast to the peripheral ossifying fibroma, the peripheral odontogenic fibroma is a rare lesion.

No specific gender predilection while the ages of the patients ranged from 5 to 65 years.commonly seen in mandible than maxilla.

slow growing, solid, firmly attached gingival mass sometimes arising between teeth and sometimes displacing teeth.

consists of cellular fibrous connective tissue parenchyma with non neoplastic islands, strands of clouman or cuboidal odontogenic epithelium.

Gingival cyst (or dental lamina cyst) is a type of cysts of the jaws that originates from the dental lamina and is found in the mouth parts. It is a superficial cyst in the alveolar mucosa. It can be seen inside the mouth as small and whistish bulge. Depending on the ages in which they develop, the cysts are classsfied into gingival cyst of newborn (or infant) and gingival cyst of adult. Structurally, the cyst is lined by thin epithelium and shows a lumen usually filled with desquamated keratin, occasionally containing inflammatory cells. The nodes are formes as a result of cystic degeneration of epithelial rests of the dental lamina (called the rests of Serres).

Gingival cyst was first described by a Czech physician Alois Epstein in 1880. In 1886, a German physician Heinrich Bohn described another type of cyst. Alfred Fromm introduced the classification of gingival cysts in 1967. According to him, gingival cysts of newborns can be further classsified based on their specific origin of the tissues as Epstein’s pearls, Bohn’s nodules and dental lamina cysts.

Bleeding on probing which is also known as bleeding gums or gingival bleeding is a term used by dentists and dental hygienists when referring to bleeding that is induced by gentle manipulation of the tissue at the depth of the gingival sulcus, or interface between the gingiva and a tooth. Bleeding on probing, often abbreviated BOP, is a sign of inflammation and indicates some sort of destruction and erosion to the lining of the sulcus or the ulceration of sulcular epithelium. The blood comes from lamina propria after the ulceration of the lining.

Atypical hyperplasia is a benign (noncancerous) cellular hyperplasia in which cells show some atypia. In this condition, cells look abnormal under a microscope and are increased in number.

Breast cancer risk is elevated for defined fraction of lesions. Except for patients with a strong family history of breast cancer, where the risk is two-fold, nonproliferative lesions have no increased risk. Proliferative lesions also have approximately a 2-fold risk. In particular, atypical hyperplasia is associated with an increased risk of developing breast cancer. Atypical lobular hyperplasia is associated with the greatest risk, approximately 5-fold and especially high relative risk of developing premenopausal breast cancer. Atypical ductal hyperplasia is associated with 2.4-fold risk. In contrast, a New England Journal of Medicine article states that for women with a strong familial history of breast cancer, the risk of future breast cancer is roughly doubled, independent of histological status. The article further states "The relative risk of breast cancer for the cohort was 1.56 (95 percent confidence interval, 1.45 to 1.68), and this increased risk persisted for at least 25 years after biopsy. The relative risk associated with atypia was 4.24 (95 percent confidence interval, 3.26 to 5.41), as compared with a relative risk of 1.88 (95 percent confidence interval, 1.66 to 2.12) for proliferative changes without atypia and of 1.27 (95 percent confidence interval, 1.15 to 1.41) for nonproliferative lesions. The strength of the family history of breast cancer, available for 4808 women, was a risk factor that was independent of histologic findings. No increased risk was found among women with no family history and nonproliferative findings. In the first 10 years after the initial biopsy, an excess of cancers occurred in the same breast, especially in women with atypia."

It is not well understood whether the lesions are precursors of breast cancer or only indication of increased risk, for most types of lesions the chance of developing breast cancer is nearly the same in the affected and unaffected breast (side) indicating only coincidence of risk factors. For atypical lobular hyperplasia there is high incidence of ipsilateral breast cancers indicating a possible direct carcinogenetic link.

Atypical hyperplasia is a high-risk premalignant lesion of the breast. It is believed that atypical ductal hyperplasia (ADH) is a direct precursor for low-grade mammary ductal carcinoma, whereas atypical lobular hyperplasia (ALH) serves as a risk indicator.

Gingival cyst of adult is a rare condition. The incidence is less than 0.5%. It is formed from the rests of dental lamina. It is found in the soft tissues on the buccal and labial portions of the jaw. It usually occurs on the facial gingiva as a single small flesh colored swelling, sometimes with a bluish hue due to the cystic fluid. Sometimes, it may occur in cluster, either unilaterally or bilaterally or on the lingual surface of the alveolar process. It is most commonly seen in the canine and premolar regions of the mandible, and are sometimes confused with lateral periodontal cysts. It is not normally problematic, but when it grows larger, it can cause some discomfort. It can be removed by simple surgical excision. They are developed late in life, generally up to the sixth decade of age.

Familial acanthosis may arise as a result of an autosomal dominant trait, presenting at birth or developing during childhood.